中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
7期
1578-1581,封4
,共5页
朱晓文%王欣%朱尤庆%陈志芬%兰海%吴洲清%陈家宽
硃曉文%王訢%硃尤慶%陳誌芬%蘭海%吳洲清%陳傢寬
주효문%왕흔%주우경%진지분%란해%오주청%진가관
调节性T细胞%转录因子叉头框蛋白p3%信号转导与转录激活因子%结直肠癌%肿瘤免疫
調節性T細胞%轉錄因子扠頭框蛋白p3%信號轉導與轉錄激活因子%結直腸癌%腫瘤免疫
조절성T세포%전록인자차두광단백p3%신호전도여전록격활인자%결직장암%종류면역
Regulatory T cell%Forkhead box P3%Signal transducers and activators of transcription 3%Colorectal cancer%Tumor immunity
目的 探讨CD4+ CD25+叉头框蛋白p3(Fox#)+调节性T细胞在结直肠癌中抑制肿瘤免疫的机制.方法 收集结直肠癌组织48例,息肉组织22例,正常组织21例,采用免疫组织化学法检测Foxp3+调节性T细胞及白细胞介素(IL)-10阳性肿瘤细胞在上述组织中的含量;逆转录-聚合酶链反应(RT-PCR)法检测Foxp3及信号转导与转录激活因子(STAT3) mRNA在不同组织中的基因表达,同时采用,检验分析上述指标与肿瘤临床病理特征之间的关系.结果 Foxp3及IL-10在结直肠癌组织中阳性细胞表达率分别为45.8%和68.8%,较息肉组织(13.6%和31.8%)及正常组织(9.5%和23.8%)显著升高(P<0.01);肿瘤组织中Foxp3及STAT3 mRNA的相对表达量分别为0.644±0.059、0.343±0.036,较息肉组织(0.322±0.020、0.212±0.028)及正常组织(0.309±0.016、0.202±0.021)明显升高(P<0.01);结直肠癌组织中Foxp3与STAT3基因表达量呈正相关(r =0.526,P<0.05),Foxp3与IL-10蛋白表达呈正相关(r=0.314,P<0.05);肿瘤组织中Foxp3的表达量与组织学分级、淋巴结转移、TNM分期明显相关(P<0.05),与年龄、性别无明显相关(P>0.05).结论 CD4+ CD25+ Foxp3+调节性T细胞通过Foxp3及其他相关抑制性细胞因子的表达抑制肿瘤免疫,进而引起肿瘤免疫逃逸,从而促进肿瘤的发生发展.
目的 探討CD4+ CD25+扠頭框蛋白p3(Fox#)+調節性T細胞在結直腸癌中抑製腫瘤免疫的機製.方法 收集結直腸癌組織48例,息肉組織22例,正常組織21例,採用免疫組織化學法檢測Foxp3+調節性T細胞及白細胞介素(IL)-10暘性腫瘤細胞在上述組織中的含量;逆轉錄-聚閤酶鏈反應(RT-PCR)法檢測Foxp3及信號轉導與轉錄激活因子(STAT3) mRNA在不同組織中的基因錶達,同時採用,檢驗分析上述指標與腫瘤臨床病理特徵之間的關繫.結果 Foxp3及IL-10在結直腸癌組織中暘性細胞錶達率分彆為45.8%和68.8%,較息肉組織(13.6%和31.8%)及正常組織(9.5%和23.8%)顯著升高(P<0.01);腫瘤組織中Foxp3及STAT3 mRNA的相對錶達量分彆為0.644±0.059、0.343±0.036,較息肉組織(0.322±0.020、0.212±0.028)及正常組織(0.309±0.016、0.202±0.021)明顯升高(P<0.01);結直腸癌組織中Foxp3與STAT3基因錶達量呈正相關(r =0.526,P<0.05),Foxp3與IL-10蛋白錶達呈正相關(r=0.314,P<0.05);腫瘤組織中Foxp3的錶達量與組織學分級、淋巴結轉移、TNM分期明顯相關(P<0.05),與年齡、性彆無明顯相關(P>0.05).結論 CD4+ CD25+ Foxp3+調節性T細胞通過Foxp3及其他相關抑製性細胞因子的錶達抑製腫瘤免疫,進而引起腫瘤免疫逃逸,從而促進腫瘤的髮生髮展.
목적 탐토CD4+ CD25+차두광단백p3(Fox#)+조절성T세포재결직장암중억제종류면역적궤제.방법 수집결직장암조직48례,식육조직22례,정상조직21례,채용면역조직화학법검측Foxp3+조절성T세포급백세포개소(IL)-10양성종류세포재상술조직중적함량;역전록-취합매련반응(RT-PCR)법검측Foxp3급신호전도여전록격활인자(STAT3) mRNA재불동조직중적기인표체,동시채용,검험분석상술지표여종류림상병리특정지간적관계.결과 Foxp3급IL-10재결직장암조직중양성세포표체솔분별위45.8%화68.8%,교식육조직(13.6%화31.8%)급정상조직(9.5%화23.8%)현저승고(P<0.01);종류조직중Foxp3급STAT3 mRNA적상대표체량분별위0.644±0.059、0.343±0.036,교식육조직(0.322±0.020、0.212±0.028)급정상조직(0.309±0.016、0.202±0.021)명현승고(P<0.01);결직장암조직중Foxp3여STAT3기인표체량정정상관(r =0.526,P<0.05),Foxp3여IL-10단백표체정정상관(r=0.314,P<0.05);종류조직중Foxp3적표체량여조직학분급、림파결전이、TNM분기명현상관(P<0.05),여년령、성별무명현상관(P>0.05).결론 CD4+ CD25+ Foxp3+조절성T세포통과Foxp3급기타상관억제성세포인자적표체억제종류면역,진이인기종류면역도일,종이촉진종류적발생발전.
Objective To study the mechanism of CD4 + CD25 + forkhead box P3 (Foxp3) + regulatory T cells inhibiting the tumor immunity in colorectal cancer.Methods Thirty-two cases of colorectal carcinoma,21 cases of polypus,and 18 cases of normal tissues were collected.T he immunohistochemistry was used to measure the number of Foxp3 + regulatory T cells and interleukin (IL)-10 positive cells in above tissues,and reverse transcription-polymerase chain reaction (RT-PCR) was done to dectect the expression of Foxp3 and signal transducers and activators of transcription 3 (STAT3) mRNA in different tissues.The relationship between the above indexes and clinicopathological features was analyzed.Results The expression rate of positive cells of Foxp3 and IL-10 in colorectal cancer was respectively 45.8% and 68.8%,significantly higher than in the polypus tissues (13.6% and 1.8%) and normal tissues (9.5%and 23.8%) (P <0.01 for all).The relative expression amount of Foxp3 and STAT3 mRNA in tumor tissue was respectively 0.644 ± 0.059 and 0.343 ± 0.036,which was significantly increased as compared with polypus (0.322 ±0.020 and 0.212 ±0.028) and normal tissue (0.309 ±0.016 and 0.202 ±0.021)(P <0.01 for all).The Foxp3 mRNA expression in colorectal cancer tissues was positively correlated with STAT3 (r =0.526.P < 0.05).The Foxp3 protein expression wass positively correlated with IL-10 (r =0.314,P < 0.05).The expression of Foxp3 in cancer patients was visibley correlated with the histological grade,lymph node metastasis and TNM stage (P < 0.05),and there was no visible correlation with age and gender (P > 0.05).Conclusion CD4 + CD25 + Foxp3 + regulatory T cells inhibit tumor immunity and induce tumor immune escape through the expression of Foxp3 and some other related inhibitory cytokines,and finally promote the tumor progression.